Physiology Of Tissue Healing PDF

Physiology of Tissue Healing Joosung Kim, PhD, ATC Injury Definition of inflammation Inflammatory response Localized responses that have cardinal signs 5 Cardinal signs Rubor: redness Calor: heat Edema: swelling Dolor: pain Funca laesa: functional...

Physiology of Tissue Healing Joosung Kim, PhD, ATC Injury Definition of inflammation Inflammatory response Localized responses that have cardinal signs 5 Cardinal signs Rubor: redness Calor: heat Edema: swelling Dolor: pain Funca laesa: functional loss  Is inflammation bad? → Essential in tissue Misconception of inflammation repair and reorganization and its dual functions Dual Functions Soldier Cleaner Phases of healing The normal tissue healing involves four main healing phases, but they are overlapped. Phase 1: Hemostasis Phase 2: Inflammatory phase Phase 3: Proliferative phase Phase 4: Remodeling Phase 1: Hemostasis (Immediate) Hemostasis is the first response to injury, and it prevents blood loss. Immediate after an injury, blood vessel constricts. Injury to skin activate platelet aggregation to form the clot (temporary patch). Plasmin digests the fibrin threads in the clot and dissolves the clot to clear away old clots. The primary action of the hemostasis is to clot the wound. Phase 2: Inflammation (1-4 days) Blood vessels dilate and the walls become more permeable. White blood cells migrate: Neutrophils appear at the injury site, cleanse debris and bacteria. Macrophases (aka “big eater”) appear next and accumulate/ facilitate the cleanup process of debris and bacteria and dead cells. Cytokines and growth factors are released and attract cells to site. Five signs of the inflammation are redness, swelling, heat, pain and loss of function.  Injury Ultrastructure (cellular) change 8 sequential Chemical mediation and Hemodynamic changes overlapping events of Metabolic changes inflammations Permeability changes Leukocyte migration Phagocytosis 1-Injury Excessive physical force is required to affect body’s structure. Factors that increase an injury risk o Physical agent ▪ Force: excessive physical force ▪ Duration ▪ Positional ▪ Postural ▪ Burn and radiation o Metabolic processes: ischemia and hypoxia o Biologic: bacteria, viruses, parasite o Chemical: acids, gases, solvent Example) stress-strain curve Primary vs. secondary Acute vs. chronic  Destruction of fine structures, especially within the cell Destruction of cell membrane and organelle. Ultrastructure change Two factors for ultrastructural change Primary: direct physical force (initial) Secondary: indirect condition associated with cell death to metabolites and/or chemical injury. Chemical mediators Histamine, bradykinin, cytokine (pro-inflammatory: IL-6 and IL-8), and anti-inflammatory cytokine (IL-10) o Chemical mediators play a role as police cops in the event of a car accident. o Histamine and Bradykinin increase permeability by pulling away the endothelium gap. ▪ Histamine: increasing vasodilation and permeability of blood vessels ▪ Bradykinin: increasing permeability and stimulate pain receptors o Cytokines Chemical mediators are activated and signaling the body that there is damage. We need to act quickly to take care of the scene. They remove and repair. White Blood Cell (Leukocyte) Hemodynamic changes Before injury After injury  Leukocyte migration FIGURE 5.4. Hemodynamic changes and leukocyte migration. (a) The leukocyte moves to the margin of the blood vessel. It then (b) sticks to the endothelium (pavementing), (c) moves over the endothelium surface, (d) finds an endothelial gap, (e) passes through the gap, and (f) leaves the vessel. (g) The leukocyte moves about in the tissue. Note, RBC is red blood cells. Hypoxia o Hypoxia = deprivation of oxygen (cells receive less oxygen) o Hypoxia forces the body to rely on anaerobic metabolism or glycolysis for energy o Anaerobic metabolism produces lactic acid buildup as Pyruvate is converted into lactate due to a lack of oxygen. o Energy efficiency decreases due to glycolysis, which produces only 2 ATP molecules per glucose molecule in comparison with 30-32 ATP in aerobic respiration. o Intracellular acidosis (too much acid in its fluid, making it more acidic than normal) leads to a slowdown of cell membrane function and inflammatory responses. Edema Phase 3: Proliferative phase (days to weeks) Proliferation means to grow or increase, indicating tissue rebuilding and formation. The wound encompasses fibroblasts that produce collagen and forming a granulation tissue (new tissue). New blood vessels form, and, in this stage, the granulation tissue appear a color of pink. Epithelial cells migrate over the wound and form a protective barrier. Phase 4: Remodeling phase (weeks to months/years) Collagen remodels and give its strength over the wound area. Scar gradually becomes flatter, stronger over time. Through the remodeling phase. Some elasticity recovers but it is not 100% return (less elastic) compared to the previous level. Summary of the tissue healing Hemostasis Vasoconstriction Clotting Inflammation Action of white blood cells Proliferation New tissues and blood vessels formation Protective barrier Remodeling Collagen remodeling Return of elasticity General tissue-healing time Skin Days – months Exercise-Induced Muscle Soreness 0-3 days Muscle Strain Grade 1: 0 – 5 weeks Grade 2: 3 week – 3 months Grade 3: 5 weeks – 6 months Tendon Injury 3 – 7 weeks Ligament Sprain Grade 1: 4 days – 5 weeks Grade 2: 3 weeks – 6 months Grade 3: 5 weeks – 8 months Bone 5 weeks – 3 months  Soft Tissue Adaptations Atrophy- a decrease in the size of tissue due to cell death and re-absorption or decreased cell proliferation Hypertrophy - an increase in the size of tissue without necessarily changing the number of cells Dysplasia - abnormal development Hyperplasia - excessive development Cartilage Healing Limited capacity to heal Little or no direct blood supply Chrondrocyte and matrix disruption result in variable healing. Is damage to cartilage alone or also to subchondral bone? Healing = Approx. 2 months  Ligament Healing bone to bone Surgically repaired ligaments tend to be stronger due to decreased scar formation vs. non-repaired ligaments Exercised ligaments are stronger Exercise vs. Immobilization Muscles must be strengthened to reinforce the joint Increased tension will increase joint stability Full healing may require 12 months Skeletal Muscle Healing Initial bleeding followed by proliferation of ground substance and fibroblast Myoblastic cells form = regeneration of new myofibrils Collagen will mature and orient along lines of tension Healing could last 6-8 weeks  TendonHarvester Tendon Healing bone to muscle Requires dense fibrous union of separated ends Abundance of collagen is required for good tensile strength Too much = fibrosis, may interfere with gliding smooth motion Week 2 - injured tendon will adhere to surrounding tissues Week 3 – tendon will gradually separate some from surrounding structures 4-5 wks before tissue can resist strong tension Tendon_both_repaired_DSCN1768  Nerve Healing Nerve cell cannot regenerate after injury (death) Regeneration can take place within a peripheral nerve fiber (outside the CNS) The closer an injury is to the cell body the harder to heal Rate of healing occurs at 3-4 mm per day Injured central nervous system nerves do not heal as well as peripheral nerves Bone Healing Acute fractures have 5 stages Hematoma formation Cellular proliferation Callus formation Ossification Remodeling  Acute Fracture Management Must be appropriately immobilized, until X-rays reveal the presence of a hard callus Fractures can limit participation for weeks or months http://i.telegraph.co.uk/multimedia/archive/02445/stoddart_2445174b.jpg https://www.youtube.co m/watch?v=i28yrh5WS bA Return to play time after injury Ligament High ankle sprain: the overall mean RTP is 52 days Surgically treated patients requires 1.5 times longer than non- surgical patients. ACL-reconstruction: RTP rate ranges from 77% to 88% and the mean time to RTP ranges from 6 to 13 months. Muscle Hamstring strain takes at least 3 weeks to 8 weeks with 90% to 100% success return rate without re-injury. Bone Tibial shaft fracture takes 54 weeks after surgery and longer after nonsurgical management. The length of the healing period depends on the fracture site Factors that affect healing Treatment modalities Drugs Surgical repair Patients age Disease Injury size Infection Nutrition Spasm Swelling Purposes of therapeutic rehabilitation Would healing Pain relief Flexibility and range of motion Muscular strength Muscular endurance Muscular speed Muscular coordination or skill Muscular power Agility Cardiorespiratory endurance Inflammatory phase Treatment goals: managing acute symptoms Control infection Manage pain Minimize swelling/hemorrhaging Promote optimal healing conditions Important & necessary step (we want inflammation) Only bad if it lasts too long Literature on NSAIDS  Management Concepts Drug utilization Antiprostaglandin agents used to combat inflammation and pain Non-steroidal anti-inflammatory agents NSAID’s Medications will work to decrease vasodilatation and capillary permeability Proliferative phase Treatment goals: continuing light activity Promote optimized tissue formation Maintain joint mobility Manage pain and swelling Strengthen surrounding muscles Protect from early-return Remodeling/maturation Wound healing continues Alignment of tissue/tensile strength Treatment goals: Promote optimized tissue formation Restore muscle strength Restore muscle endurance Restore muscle power Return to ADL’s Return to activity Gradual progressive loading Still being aware of when changing mechanical loads can be increased (avoid quick changes)  Pain Major indicator of injury Pain is individual and subjective Factors involved in pain Anatomical structures Physiological reactions Psychological, social, cultural and cognitive factors Types Acute, Chronic, Referred Pain Categories Pain sources Fast versus slow pain Acute versus chronic Projected or referred pain © 2011 McGraw-Hill Higher Education. All rights reserved. Pain Transmission Pain picked up by nociceptors Afferent nerves transmit impulse to brain Impulse is interpreted and acted upon  Treating Pain Must break pain-spasm-hypoxia-pain cycle through treatment Agents used: Immobilization Heat/cold Electrical stimulation-induced analgesia Manual therapies Pharmacological agents  Modalities Used to relieve pain and control other s/s Introduce thermal agents for pain control Utilize electrical modalities to reduce pain TENS and acupuncture commonly used to target Gate Theory Manual therapies (massage, SCS, myofascial release) Pharmacological Agents Oral, injectable medications Commonly analgesics and anti-inflammatory agents Reflections Effects of injury The inflammatory response and its cardinal signs The eight inflammatory events and details Misconceptions about inflammation Hypoxia Edema Four main phases of tissue healing. Various timelines for different types of tissues. Severity of sports injury for the recovery. Pain Treatment goals according to healing phases. Factors affecting the healing